Developmental and genetic audiogenic seizure models: behavior and biological substrates

Citation
Kc. Ross et Jr. Coleman, Developmental and genetic audiogenic seizure models: behavior and biological substrates, NEUROSCI B, 24(6), 2000, pp. 639-653
Citations number
150
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
ISSN journal
01497634 → ACNP
Volume
24
Issue
6
Year of publication
2000
Pages
639 - 653
Database
ISI
SICI code
0149-7634(200008)24:6<639:DAGASM>2.0.ZU;2-1
Abstract
Audiogenic seizure (AGS) models of developmental or genetic origin manifest characteristic indices of generalized seizures such as clonus or tonus in rodents. Studies of seizure-resistant strains in which AGS is induced by in tense sound exposure during postnatal development provide models in which o ther neural abnormalities are not introduced along with AGS susceptibility. A critical feature of all AGS models is the reduction of neural activity i n the auditory pathways from deafness during development. The initiation an d propagation of AGS activity relies upon hyperexcitability in the auditory system, particularly the inferior colliculus (IC) where bilateral lesions abolish AGS. GABAergic and glutaminergic mechanisms play crucial roles in A GS, as in temporal lobe models of-epilepsy, and participate in AGS modulato ry and efferent systems including the superior colliculus, substantia nigra , basal ganglia and structures of the reticular formation. Catecholamine an d indolamine systems also influence AGS severity. AGS models are useful for elucidating the underlying mechanisms for formation and expression of gene ralized epileptic behaviors, and evaluating the efficacy of modern treatmen t strategies such as anticonvulsant medication and neural grafting. (C) 200 0 Elsevier Science Ltd. All rights reserved.